Why is a series of articles on neuropsychological and neurological impairments in various psychopathologic conditions worth putting together for a special issue of Psychiatric Clinics of North America? Over the course of my career as a neuropsychologist, I can only estimate the number of times (surely in the thousands!) I have received a referral that includes some version of the question: “Is there an organic component?” for patients with a psychiatric diagnosis. No one appreciated it when I scrawled back “yes” on the referral form, without doing any cognitive testing. Because even today I occasionally receive the functional versus organic question at the state psychiatric hospital where I work, I decided that putting this issue together to describe the evidence for brain involvement in psychiatric disorders would be a worthy project.
In an effort to describe what is and is not known, this issue attempts to address seven of the most common and disruptive psychiatric disorders from the fourth edition of the Diagnostic and Statistical Manual (DSM-IV). The authors were asked to address the following questions:
1.Is there anything specific about the profile of cognitive impairment in this disorder?
2.If there are specific findings, how do these impairments relate to the underlying psychopathology/neuroanatomy of the disorder?
3.Is there a progressive component to the disorder, or evidence that the cognitive and neurological impairment changes over the course of the disorder?
4.What impact do these impairments have in terms of treatment implications (psychopharmacology, cognitive rehabilitation, or psychotherapy)?
The authors took different approaches to answering these questions, in part based on available literature and research knowledge. In the first article, on schizophrenia, Flashman et al discuss the fact that there is no pathognomic neuropsychological or structural neuroanatomic profile, although several studies have indicated that verbal episodic memory and vigilance deficits are particularly prominent and are observed even in untreated patients in their first episode of the disorder. The course of schizophrenia appears variable, and factors that contribute to the development of the illness, and in some patients, to deterioration of cognitive functioning, have not been elucidated clearly. Marvel and Paradiso describe cognitive symptoms frequently observed in affective disorders, including poor attention, memory and executive function. Neuroimaging studies indicate that these impairments in both patient populations may be related to disruptions of the dorsal lateral and ventral medial prefrontal cortex. Neurological symptoms are predominantly motor-related and often involve psychomotor retardation. The deficits reported range in severity and often are associated with decrements in mood status. Not all symptoms, however, follow this pattern, and many cognitive symptoms remain present even in the euthymic phase of the illness.
The neuropsychological deficits in obsessive–compulsive disorder (OCD), consisting primarily of executive deficits, appear to involve frontal–striatal systems dysfunction (see Anderson and Savage). Neuroimaging studies suggest that orbitofrontal cortex and caudate abnormalities may play a role. Additional information about the neurobiology of OCD comes from assessment of neurological soft signs, which suggest complex brain dysfunction. Kimble and Kaufman discuss the role of four critical neural systems (including the locus coeruleus, the hippocampus, the amygdala, and the thalamus) in post-traumatic stress disorder, in an effort to understand the more prominent responses to trauma, such as hyperarousal, memory disturbance, and dissociation. Monarch et al point out that while borderline personality disorder (BPD) is not considered routinely a neurocognitive disorder, neuropsychological studies suggest that particular weaknesses in attention–vigilance and verbal learning and memory have been noted in these patients. Studies also reveal a higher prevalence of neurological soft signs and electroencephalogram (EEG) abnormalities in BPD patients. Structural imaging studies generally do not report abnormalities associated with BPD; functional imaging studies indicate significant hypermetabolism in prefrontal and frontal regions and significant hypometabolism in the hippocampus in patients with BPD compared with healthy controls. Roth and Saykin report that neuropsychological studies have shown several cognitive disturbances in children and adults with attention-deficit/hyperactivity disorder (ADHD). Executive dysfunction is particularly prominent. Neuroimaging investigations have as a result targeted frontal-striatal-thalamic-cortical (FSTC) circuitry. Structural MRI studies note changes in frontal lobe and striatum and in the cerebellum and corpus callosum. Functional imaging studies have reported abnormal blood flow and dopamine receptor binding in FSTC circuitry patients with ADHD while at rest, and abnormal activation of FSTC when performing executive function tasks.
Finally, in the review by Vik et al, cognitive deficits associated with common drugs of abuse are presented. As they note, acute intoxication and immediate and protracted withdrawal often produce transient alterations of cognitions that persist for weeks to months. In fact, some residual effects remain for up to 1 year. Surprisingly, evidence of irreversible effects is less clear. In addition, the authors discuss critical periods of exposure to drug use and summarize treatment implications for psychoactive substance users.
As can be seen from this brief synopsis, there is strong evidence of neurological and cognitive dysfunction in disorders that typically are considered psychiatric. Although the range of cognitive problems can be quite diverse, there are several cognitive domains, including executive, attentional, and memory, that appear most frequently at risk, although there is a broad range of impairment across and within the psychiatric disorders highlighted in this issue. Further, despite a diversity of candidate regions involved in the neuroanatomic/neurologic presentation of these disorders, particular brain regions frequently are implicated. Frontal lobe, thalamus, basal ganglia, hippocampus are mentioned repeatedly in these reviews. Without a doubt, there is more to be learned about the specificity of neurologic and cognitive impairment across disorders, the relationship of these deficits to the underlying psychopathology/neuroanatomy of the disorders, and the impact of the impairments on treatment implications. Further advances in neuroimaging techniques and more precise measurement of neuropsychological abilities will continue to help unlock the secrets of the brain and its role in psychiatric illness. I look forward to seeing an update in the next 5 years.